Gabor G Kovacs,Yuriko Katsumata,Xian Wu,Khine Zin Aung,David W Fardo,Shelley L Forrest,,Peter T Nelson
{"title":"以淀粉样蛋白-β为主的阿尔茨海默病神经病理变化。","authors":"Gabor G Kovacs,Yuriko Katsumata,Xian Wu,Khine Zin Aung,David W Fardo,Shelley L Forrest,,Peter T Nelson","doi":"10.1093/brain/awae325","DOIUrl":null,"url":null,"abstract":"Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread Aβ plaques but no/mild tau tangles (Aβ-predominant ADNC, or AP-ADNC), may have distinct genetic and clinical features. Analyzing National Alzheimer's Coordinating Center data, we stratified 1,187 participants into AP-ADNC (n = 95), low Braak primary age related tauopathy (PART; n = 185), typical-ADNC (n = 832), and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT, and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.","PeriodicalId":9063,"journal":{"name":"Brain","volume":null,"pages":null},"PeriodicalIF":10.6000,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Amyloid-β predominant Alzheimer's disease neuropathologic change.\",\"authors\":\"Gabor G Kovacs,Yuriko Katsumata,Xian Wu,Khine Zin Aung,David W Fardo,Shelley L Forrest,,Peter T Nelson\",\"doi\":\"10.1093/brain/awae325\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread Aβ plaques but no/mild tau tangles (Aβ-predominant ADNC, or AP-ADNC), may have distinct genetic and clinical features. Analyzing National Alzheimer's Coordinating Center data, we stratified 1,187 participants into AP-ADNC (n = 95), low Braak primary age related tauopathy (PART; n = 185), typical-ADNC (n = 832), and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT, and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.\",\"PeriodicalId\":9063,\"journal\":{\"name\":\"Brain\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":10.6000,\"publicationDate\":\"2024-10-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Brain\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/brain/awae325\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Brain","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/brain/awae325","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Different subsets of Alzheimer's disease neuropathologic change (ADNC), including the intriguing set of individuals with severe/widespread Aβ plaques but no/mild tau tangles (Aβ-predominant ADNC, or AP-ADNC), may have distinct genetic and clinical features. Analyzing National Alzheimer's Coordinating Center data, we stratified 1,187 participants into AP-ADNC (n = 95), low Braak primary age related tauopathy (PART; n = 185), typical-ADNC (n = 832), and high-Braak PART (n = 75). AP-ADNC differed in some clinical features and genetic polymorphisms in the APOE, SNX1, WNT3/MAPT, and IGH genes. We conclude that AP-ADNC differs from classical ADNC with implications for in vivo studies.
期刊介绍:
Brain, a journal focused on clinical neurology and translational neuroscience, has been publishing landmark papers since 1878. The journal aims to expand its scope by including studies that shed light on disease mechanisms and conducting innovative clinical trials for brain disorders. With a wide range of topics covered, the Editorial Board represents the international readership and diverse coverage of the journal. Accepted articles are promptly posted online, typically within a few weeks of acceptance. As of 2022, Brain holds an impressive impact factor of 14.5, according to the Journal Citation Reports.